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DHEA (dehydroepiandrosterone)


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One of the hormones people in withdrawal ask about is DHEA (dehydroepiandrosterone). There are a lot of questions about whether taking this or that hormone can reduce withdrawal symptoms. The answer probably is, that depends. It depends on your gender, it depends on your age, and it depends on whether you might be low in those hormones.

 

As I understand it, the level of DHEA in your body declines as you get older. It can convert to testoterone or estrogen. It is thought to convert to testosterone in women; it's unknown what it does in men.

 

It's always a good idea to talk to a doctor who understands these things and do as much research as you can before you try anything. And then, try extremely small doses. You do not want to make symptoms worse with an adverse reaction when you experiment.

 

Here is some good background information about DHEA from the Mayo Clinic:

 

http://www.mayoclinic.com/health/dhea/NS_patient-dhea/METHOD=print

 

"....There is sufficient evidence supporting the use of DHEA in the treatment of adrenal insufficiency, depression, induction of labor, and systemic lupus erythematosus.

 

No studies on the long-term effects of DHEA have been conducted. DHEA can cause higher than normal levels of androgens and estrogens in the body, and theoretically may increase the risk of prostate, breast, ovarian, and other hormone-sensitive cancers. Therefore, it is not recommended for regular use without supervision by a licensed health professional. ...."

 

 

Cautions on DHEA -- it is, after all, a quasi-steroid or hormone like testosterone or estrogen.

 

According to the Physician's Desk Reference in 2006:

 

CONTRAINDICATIONS

 

DHEA supplementation is contraindicated in those with prostate, breast, uterine and ovarian cancer.

 

PRECAUTIONS

 

DHEA supplementation should be avoided by children, adolescents, pregnant women and nursing mothers.

 

ADVERSE REACTIONS

 

Various androgenic effects, including acne, deepening of the voice, hirsutism and hair loss have been reported in women using supplemental DHEA. There is a report of transient hepatitis associated with DHEA use by a woman. Decreased HDL-cholesterol levels have been reported in women using oral DHEA. This could increase risk of cardiovascular disease. Elevated IGF (insulin-like growth factor)-1 levels have been noted in both men and women taking oral DHEA. Elevated IGF-1 levels have been associated with increased risk of certain types of cancer, e.g. prostate cancer. Oral DHEA has also been observed to increase insulin resistance when taken by women.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

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From the Life Enhancement Foundation:

 

http://www.life-enhancement.com/article_template.asp?ID=264

 

Mechanisms by which DHEA is thought to elevate mood or yield antidepressant effects include:

- Greater production of testosterone and estrogen (each of these hormones has been associated with elevation in mood).

- Increased bioavailability of testosterone by alteration of albumin's affinity for testosterone. (DHEA is thought to increase the ability of albumin, a blood protein, to carry testosterone to where it is needed in the body, and this is associated with mood elevation, as explained in the prior item.)

- Antagonism of the negative effects of cortisol (an adrenal hormone that, in excessive amounts or if imbalanced with DHEA, is associated with age-related pathology).

- Modulation of GABA receptors (GABA is a buffering neurotransmitter associated with sedation).

- Alteration of NMDA neurotransmission (NMDA is a neurotransmitter that can produce neurotoxic effects under certain circumstances).

- Binding to sigma receptors (sigma receptors are associated in the brain with excessive stimulation, which may cause neurotoxic effects under certain circumstances).

- Increased serotonin levels in specific areas of the brain, thereby increasing natural sedation.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

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Acta Physiol Scand. 1999 Nov;167(3):181-8.

 

Neuroactive steroids: their mechanism of action and their function in the stress response.

 

Zinder O, Dar DE.

 

Department of Clinical Biochemistry, Rambam Medical Center, and the Technion, Israel Institute of Technology, Faculty of Medicine, Haifa, Israel.

 

Steroids are usually identified as genomic regulators, yet recently a body of evidence has accumulated demonstrating specific plasma membrane effects, as well as coordinative effects, of some steroids on both membrane and intracellular receptors. The resulting rapid (<1 min) modulation of cellular activity has strongly suggested a non-genomic, and possibly modulatory, role for certain steroid compounds, and dramatic effects on membranes of excitable as well as other tissues have been demonstrated. Steroid synthesis and metabolism have been shown to exist in the CNS, and the effects have been seen in both the central and peripheral nervous systems. The major groups of neuroactive steroids, and their metabolites, have been progesterone, deoxycorticosterone, and some androgens, notably dihydroxyepiandrosterone (DHEA). These compounds show increased concentrations both in blood and in the brain following stress and they have also been associated with anxiolytic effects and antiepileptic activity. In the periphery, some of these compounds show remarkable inhibitory effects on the secretion of catecholamines and other neurotransmitters. The mechanism for the majority of the effects of these steroids is via their effect on receptor-mediated binding to ligand-gated ion channels. Activation of the GABAA receptor complex, resulting in the opening of its central chloride channel, is the major target of the neuroactive steroids, resulting in re-polarization of the plasma membrane and inhibition of further neuronal firing. The anxiolytic, anti-convulsant and sedative-hypnotic actions of these neuroactive steroids have resulted in their being used as therapeutic agents for the treatment of anxiety, epilepsy, insomnia, and possibly for the alteration of pain thresholds.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

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Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4678-83.

 

Dehydroepiandrosterone: a potential signalling molecule for neocortical organization during development.

 

Compagnone NA, Mellon SH.

 

Source

 

Reproductive Endocrinology Center, Department of Obstetrics, Gynecology, and Reproductive Sciences, and The Metabolic Research Unit, University of California, San Francisco, CA 94143-0556, USA.

 

Abstract and full text at http://www.ncbi.nlm.nih.gov/pubmed/9539798

 

Dehydroepiandrosterone (DHEA) and its sulfate derivative (DHEAS) are the most abundant steroids produced by the human adrenal, but no receptors have been identified for these steroids, and no function for them has been established, other than as precursors for sex steroid synthesis. DHEA and DHEAS are found in brains from many species, and we have shown that enzymes crucial for their synthesis, especially P450c17 (17alpha-hydroxylase/c17,20 lyase), are expressed in a developmentally regulated, region-specific fashion in the developing rodent brain. One region of embryonic expression of P450c17, the neocortical subplate, has been postulated to play a role in guiding cortical projections to their appropriate targets. We therefore determined if products of P450c17 activity, DHEA and DHEAS, regulated the motility and/or growth of neocortical neurons. In primary cultures of mouse embryonic neocortical neurons, DHEA increased the length of neurites containing the axonal marker Tau-1, and the incidence of varicosities and basket-like process formations in a dose-dependent fashion. These effects could be seen at concentrations normally found in the brain. By contrast, DHEAS had no effect on Tau-1 axonal neurites but increased the length of neurites containing the dendritic marker microtubule-associated protein-2. DHEA rapidly increased free intracellular calcium via activation of N-methyl-D-aspartate (NMDA) receptors. These studies provide evidence of mechanisms by which DHEA and DHEAS exert biological actions, show that they have specific functions other than as sex steroid precursors, mediate their effects via non-classic steroid hormone receptors, and suggest that their developmentally regulated synthesis in vivo may play crucial and different roles in organizing the neocortex.

 

 

 

University of California San Francisco News Office

24 April 1998

 

DHEA STIMULATES GROWTH OF BRAIN CELLS, UCSF RESEARCHERS CONCLUDE

 

Despite the popularity of popping DHEA pills among dietary supplement enthusiasts in search of a fountain of youth, the naturally occurring form of DHEA has never been shown to be anything more than a way station on the biochemical trail leading to production of more exciting compounds, such as the sex hormones testosterone and estrogen. But in the most recent (April 14) issue of the Proceedings of the National Academy of Sciences, researchers at the University of California San Francisco report that in the brains of mice -- and very likely in the brains of humans as well -- DHEA and a related, sulfur-containing version of the compound, called DHEAS, can stimulate the growth of nerve cell fibers needed to form electrical connections in the brain.

 

In the mouse embryo, enzymes that are needed to make DHEA and DHEAS in the brain are located at brain sites where nerve cells extend branches to connect the thalamus to more highly evolved regions in the brain's cortex, the UCSF researchers have determined. Nerve cells from the cortex maintained in laboratory cultures are stimulated differently by DHEA -- short for dyhydroepiandrosterone -- and by DHEAS, according to Synthia H. Mellon, associate professor of obstetrics, gynecology and reproductive sciences at UCSF, and assistant research scientist Nathalie A. Compagnone, PhD. DHEA fosters the growth of fibers that transmit signals to other nerve cells, while DHEAS stimulates growth of fibers that receive signals from other nerve cells, the UCSF researchers discovered. These growth-stimulating properties appear in cells that undergo rapid biochemical changes in response to DHEA and DHEAS.

 

"These studies provide evidence that DHEA and DHEAS exert biological actions and are not simply sex hormone precursors," Mellon says. "The regulated production of DHEA and DHEAS in the embryonic brain may play a crucial role in organizing neural connections." "DHEA and DHEAS do not appear to be slow-acting hormones that attach to specific receptors on cells like classic hormones. Instead they cause rapid changes in nerve cells, like neurotransmitters do."

 

DHEA has primarily been thought of as a compound made by the adrenal glands, which sit atop the kidneys. The adrenal gland's production of DHEA, which is converted into sex hormones, peaks at about age 20, at higher levels in men than women. Thereafter, blood concentrations of DHEA decline steadily throughout adulthood in both sexes, typically dropping to 15 to 20 percent of youthful levels in old age. This decline has led researchers to search for an association among blood levels of DHEA, signs of aging, and diseases associated with aging.

 

In animal studies that may be relevant to investigations of memory impairment in Alzheimer's, old mice--which normally perform poorly in learning tests with mazes--were able to learn as well as young mice when given DHEA with their drinking water, according to Owen Wolkowitz, MD, a professor of psychiatry at UCSF.

 

Wolkowitz and UCSF colleague Louann Brizendine, MD, associate clinical professor of psychiatry, are now conducting clinical trials to investigate any potential benefits of DHEA in Alzheimer's patients and in individuals who are clinically depressed. In a preliminary study Wolkowitz found that depressed DHEA recipients reported improved psychological well-being and mood, and that they had better recall in tests of memory. The new research findings by Compagnone and Mellon raise many questions about the role of DHEA and the related sulfur-containing compound, DHEAS, in normal brain development, in the maintenance of brain function in adulthood and in neurodegenerative diseases such as Alzheimer's. It also is not clear if DHEA and DHEAS made by the human adrenal gland act on the brain, or whether the brain continues to make its own supply of these steroids after the framework for the brain's neural architecture is completed about a year after birth, Mellon says.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

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http://www.medscape.com/viewarticle/406925

 

DHEA: Dehydroepiandrosterone

 

Joseph Pepping, Pharm.D.

[Am J Health-Syst Pharm 57(22):2048-2056, 2000. © 2000 ASHP, Inc.]

 

Introduction

 

Dehydroepiandrosterone (DHEA) and its active metabolite, DHEA sulfate (DHEAS), are endogenous hormones synthesized and excreted primarily by the zona reticularis of the adrenal cortex in response to adrenocorticotropic hormone. The exact mechanism of action and clinical role, if any, of DHEA and DHEAS remain unclear. Epidemiological data indicate an inverse relationship between serum DHEA and DHEAS levels and the frequency of cancer, cardiovascular disease (in men only), Alzheimer's disease and other age-related disorders, immune function, and progression of HIV infection.[1] Animal (primarily rodent) studies have suggested many beneficial effects of DHEA, including improved immune function and memory and prevention of atherosclerosis, cancer, diabetes, and obesity. Many of the benefits seen in animal studies have yet to be shown in humans.[1-3]

 

Uses

 

Clinically substantiated (yet still controversial) uses of DHEA include replacement therapy in patients with low serum DHEA levels secondary to chronic disease, adrenal exhaustion, or corticosteroid therapy; treating systemic lupus erythematosus (SLE), improving bone density in postmenopausal women; improving symptoms of severe depression; improving depressed mood and fatigue in patients with HIV infection; and increasing the rate of reepithelialization in patients undergoing autologous skin grafting for burns.[1,4-8] Other possible uses (with some supporting clinical studies) include enhancing the immune response and sense of well-being in the elderly, decreasing certain cardiovascular risk factors, and treating male erectile dysfunction.[4,8-12] Use of DHEA to slow or reverse the aging process, improve cognitive function, promote weight loss, increase lean muscle mass, or slow the progression of Parkinson's disease and Alzheimer's disease is clinically unsubstantiated.[3,4,9]

 

Pharmacology

 

In women, the synthesis of DHEA and DHEAS occurs almost exclusively in the adrenal cortex, whereas in men the testes secrete approximately 5% of DHEAS and 10-25% of DHEA.[3] Minute amounts are synthesized de novo in the brain.[3,13] In young adults the adrenal cortex secretes approximately 4 mg of DHEA and 25 mg of DHEAS per day.[2] During gestation, large amounts of DHEA and DHEAS are secreted by the fetal adrenal glands. At birth, output drops to negligible amounts in both sexes and remains that way until five to seven years of age. At the onset of adrenarche, the adrenal glands gradually resume DHEA and DHEAS production, which accelerates through puberty. DHEA and DHEAS output is maximal between the ages of 20 and 30 years and then starts a decline of approximately 2% per year, leaving a residual of 10-20% of the peak production by the eighth or ninth decade of life.[2,14-16]

 

DHEA and DHEAS are interconvertible by sulfohydrolases in peripheral and adrenal tissues.[3] Some 64-74% of the DHEAS produced each day is converted to DHEA, but only 13% of the DHEA produced is metabolized to DHEAS.[2,17,18] In humans, the brain-to-plasma ratios for DHEA and DHEAS are 4-6.5 and 8.5, respectively, indicating a neuroendocrine role for these hormones.[2,19,20]

 

DHEA and DHEAS serve as the precursors of approximately 50% of androgens in men, 75% of active estrogens in premenopausal women, and 100% of active estrogens after menopause.[2,16] There appears to be a sex-specific response to DHEA replacement therapy in humans. In postmenopausal women (ages 50-65), supraphysiological doses of 100 mg of DHEA per day have predominantly androgenic effects, increasing testosterone levels approximately 300% over baseline levels.[21] In older men (mean ± S.D. age, 58.8 ± 5.1 years), 100 mg/day did not affect testosterone or dihydrotestosterone levels, but 17 beta-estradiol and estrone levels were increased over baseline by 37% and 225%, respectively (p < 0.0001 for both).[22] It has been hypothesized that the increase in serum estrogens may provide a mechanism for beneficial cardiovascular effects in men; however, clinical studies addressing the possible cardioprotective effects of DHEA have been inconclusive.

 

Several mechanisms of action of DHEA and DHEAS other than their role as precursors of the sex hormones have been proposed. In the central nervous system, both DHEA and DHEAS appear to affect neurotransmitter receptors. In rodents, DHEAS binds to the -aminobutyric acid (GABA)/benzodiazepine-receptor complex (GABA-RC) and acts as a negative noncompetitive modulator of GABA-RC. DHEA, on the other hand, appears to have GABA-agonist effects on the GABA-RC. DHEA selectively enhances the neuronal response to N-methyl- D-aspartate.[3,4] Also, DHEA and DHEAS appear to have neurotrophic effects, increasing the number of neurofilament-positive neurons and regulating the motility and growth of corticothalamic projections in cultured mouse embryo brain cells.[23-25]

 

Supraphysiological oral doses of DHEA (100-300 mg/day) in humans have been found to inhibit the synthesis of thromboxane A 2 in activated platelets, reduce plasma plasminogen activator inhibitor type 1 and tissue plasminogen activator antigen, increase serum levels of insulin-like growth factor 1 (IGF-1), and increase cyclic guanosine monophosphate and nitric oxide synthesis (either directly or via increased levels of IGF-1).[4,26-28] These effects suggest that DHEA may be beneficial in improving circulation in the microvasculature and regulating some of the risk factors of cardiovascular disease, such as platelet aggregation and ischemia. Clinical studies in this area have been equivocal, with a majority showing an inverse relationship between DHEA or DHEAS levels and cardiovascular morbidity and mortality in men but not in women.[29] However, a recently published five-year epidemiologic cohort study found no statistically significant correlation between serum DHEA or DHEAS levels and the development of atherosclerosis in men or women.[30]

 

DHEA may play a positive role in modulation of the immune response. Clinical studies in elderly persons have demonstrated that oral DHEA doses of 50 mg/day increase IGF-1 levels (p < 0.01) and cause functional activation of T cells (increases in CD8+ and CD56+ cells [natural killer cells] and enhanced cytotoxic activity).[4,9,31,32] Serum levels of interleukin- 6 (a proinflammatory cytokine involved in the pathogenesis of osteoporosis, rheumatoid arthritis, atherosclerosis, Alzheimer's disease, Parkinson's disease, and beta-cell malignancies) increase significantly with age and are inversely correlated with serum DHEA and DHEAS levels (p < 0.001). In addition, DHEA, DHEAS, and androstenedione inhibit the production of interleukin-6 by peripheral blood mononuclear cells in a concentration-dependent manner (p < 0.001).[33]

 

Pharmacokinetics

 

Oral absorption of DHEA is excellent. The volume of distribution is 17.0-38.5 L for DHEA and 8.5-9.3 L for DHEAS. DHEA and DHEAS are converted into several active metabolites, including androstenedione, testosterone, estrone, estradiol, and estriol (Figure 1). The elimination half-life of DHEA is 15-38 minutes, whereas the half-life of DHEAS is 7-22 hours. Renal excretion accounts for 51-73% of the elimination of DHEAS and its metabolites.[2,4,34-36]

 

[Figure 1.]

 

Clinical Studies

 

To date, clinical studies of DHEA in patients with specific diseases have yielded generally inconclusive results. Most of the studies were open label or had very small samples. Most of the studies discussed below were randomized, double-blind, placebo-controlled trials in which the oral dosage was 300 mg/day. Tummala and Svec [37] demonstrated that incremental increases in serum DHEA and DHEAS levels appear to plateau at an oral DHEA dosage of 300 mg/day and inferred that doses greater than this have little additional therapeutic value.

 

Postmenopausal Bone Density

 

In a randomized, double-blind, placebo-controlled study by Baulieu et al.,[10] 280 healthy men and women ages 60-79 years were given DHEA 50 mg/day orally for 12 months. Increases in bone mineral density (p < 0.05) and decreases in biochemical markers of bone turnover (p < 0.01 for serum C-terminal peptide and p < 0.05 for serum bone alkaline phosphatase) were observed at 12 months in women older than 70 but not in any other subgroup.

 

Systemic Lupus Erythematosus

 

DHEA supplementation has shown promise for the treatment of SLE. In a randomized, double-blind trial,[38,39 28] women with SLE received DHEA 200 mg/day for three months. In the DHEA group, the SLE Disease Activity Index score and both the patients' and the physicians' overall assessments of disease activity decreased, whereas small increases were seen in the placebo group. However, significance was achieved only for the visual-analogue- scale component of the index (p = 0.022). Lupus flares occurred less frequently in the treatment group than in the placebo group (three versus eight flares, p = 0.053), and a nonsignificant decrease in prednisone requirements was noted in the treatment group (from a mean ± S.D. daily dose of 12.4 ± 3.2 mg to 9.1 ± 2.3 mg, compared with an increase from 5.3 ± 1.37 mg to 7.3 ± 2.9 mg in the placebo group). Serum titers of antibodies to double-stranded DNA and levels of complement components C3 and C4 did not change significantly between the groups.

 

Well-being and Cognition

 

In a randomized, placebo-controlled, crossover trial, 30 patients ages 40-70 years were given 50 mg of DHEA orally daily.9 Within two weeks, this dose restored serum DHEA levels in both men and women to those found in young adults. With DHEA treatment, 67% of the men and 84% of the women perceived an increase in physical and psychological well-being. However, the study has been criticized for its use of an open-ended questionnaire for self-assessment of well-being.[40]

 

At present, there are no rigorous data to support an improvement in memory or other aspects of cognitive function after DHEA replacement therapy. Low endogenous levels of DHEA and DHEAS do not appear to be associated with an increased risk of dementia.[41]

 

Depression

 

The possible relationship between depression and serum DHEA and DHEAS levels is intriguing; however, more research is needed. Some authors have suggested that abnormal diurnal variations in serum DHEA and DHEAS levels, as well as abnormally high cortisol- to-DHEA ratios, may be causative factors in depression in adults and depression with comorbid panic or phobic disorders in adolescents.[3,42-44]

 

In a randomized, double-blind trial by Wolkowitz et al.,[45] 22 patients who had major depression (a Hamilton Rating Scale for Depression [HAM-D] score of 16 or greater) and who were either medication free or stabilized on antidepressant regimens received DHEA (30 mg/day for weeks 1 and 2, 60 mg/day for weeks 3 and 4, and 90 mg/day for weeks 5 and 6) or placebo. At the end of the six weeks, the mean decrease in the HAM-D score was 30.5% in the treatment group and 5.3% in the placebo group (p < 0.04). Five of 11 patients in the treatment group were considered responders (at least a 50% decrease in HAM-D score), compared with none of the 11 patients in the placebo group.

 

Effects in HIV-Infected Patients

 

In a recent open-label trial evaluating the effect of DHEA on depressed mood and fatigue, 45 HIV-positive patients (39 men and 6 women) received oral DHEA doses of 200-500 mg/day for eight weeks.[11] Of the 32 patients who completed the trial, 23 (72%) had an improvement in mood and 26 (81%) had a reduction in fatigue. There was a significant increase in body cell mass and libido but no effect on CD4+ lymphocyte counts or testosterone levels in men. The positive effects on mood, fatigue, and body cell mass continued for an additional four weeks in a subsequent double-blind phase of the study. Christeff et al.[46] have noted an inverse relationship between serum DHEA and DHEAS levels and the immunologic deterioration in HIV patients, which suggests a role for DHEA and other androgens in the normal functioning of the immune system.

 

Effects on Physical Variables

 

A randomized, double-blind, placebo-controlled crossover trial by Morales et al.[21] looked at the effects of oral DHEA 100 mg/day in 16 subjects 50-65 years of age. Baseline levels of serum DHEA, DHEAS, androstenedione, testosterone, and dihydrotestosterone were at or below the low end of the range for young adults. In both sexes, DHEA 100 mg/day restored serum DHEAS to levels at or slightly above the upper limit of the young-adult range. In women, androstenedione, testosterone, and dihydrotestosterone were increased to three to five times baseline levels (p < 0.001 for each hormone), or to levels above the sex-specific ranges for young adults, whereas in men only androstenedione was significantly increased above baseline (p < 0.05). Serum IGF-1 levels increased by a mean ± S.D. of 16% ± 6% (p = 0.04) in men and 31% ± 12% in women (p = 0.02). In men but not women, fat body mass decreased by 6.1% ± 2.6% (p = 0.02), and there were increases in knee muscle strength (15.0% ± 3.3%, p = 0.02) and lumbar back strength (13.9% ± 5.4%, p = 0.01). No changes in basal metabolic rate, bone mineral density, urinary pyridinoline cross-links, fasting insulin, glucose, cortisol, or lipids were observed in either sex.

 

Dosage

 

Physiological replacement dosages of oral DHEA in healthy people older than 40 years are in the range of 20-50 mg/day for men and 10-30 mg/ day for women.[2,4,8] These dosages are usually adequate to increase serum DH-EAS to the levels found in adults 20-30 years of age and to bestow the reported benefits of a heightened sense of well-being in both sexes, increased bone mineral density in postmenopausal women, and amelioration of erectile dysfunction in men. Higher dosages may be necessary for increasing suppressed DHEA and DHEAS levels secondary to chronic disease, adrenal exhaustion, and corticosteroid therapy. Replacement doses of DHEA are usually taken once daily in the morning.

It is imperative that serum DHEAS concentration be measured before DHEA replacement therapy is started. The serum DHEAS level should be checked at least annually to ensure that it is in the normal range. To minimize adverse effects and maximize benefits, it is suggested that replacement dosages in healthy adults be adjusted to maintain serum levels of DHEAS in the second or third quartile of sex-specific, young-adult ranges.

 

Pharmacologic dosages of 200 mg/day have been successfully used in patients with SLE. Dosages of 200-500 mg/day have been used in HIV-positive patients with depressed mood and fatigue. It is not known what effect long-term physiological or supraphysiological doses of DHEA may have on suppression of the zona reticularis of the adrenal cortex; however, there does not appear to be feedback inhibition of DHEA or DHEAS secretion by the hypothalamic-pituitary axis.[2]

 

Adverse Effects

 

Increased facial sebum production, acneiform dermatitis, and mild hirsutism have been reported in women taking DHEA in physiological or supraphysiological dosages (25-200 mg/ day).[4,21,38] Hepatitis was reported in a postmenopausal woman with preexisting high titers of antinuclear antibodies who received a single oral dose of 150 mg of DHEA; causality could not be established.[4,47] A supraphysiological dosage of DHEA (100 mg/day) was shown to increase androstenedione, testosterone, and dihydrotestosterone levels threefold to fivefold in postmenopausal women.[21] The long-term effects of these increases in androgen levels in women are not known. A nested case-control study by Dorgan et al.[48] found that postmenopausal women (not taking DHEA or hormone replacement therapy) whose levels of endogenous DHEAS were in the highest quartile had a significantly higher risk of breast cancer (risk ratio, 2.8 [95% confidence interval 1.1-7.4]) than women whose levels of endogenous DHEAS were in the lowest quartile.

 

Drug Interactions

 

Calcium-channel blockers and metformin increase levels of endogenous DHEAS, whereas corticosteroids and insulin significantly decrease them.[3] Supraphysiological dosages of DHEA can increase serum triazolam levels because of an inhibition of metabolism.[8] Theoretically, aromatase inhibitors, such as chrysin (5.7-dihydroxyflavone), an extract from the plant Passiflora coerula, can increase levels of androgens, including DHEA and DHEAS, in both men and women. Kroboth et al.[3] published an excellent review of the effects of disease, diet, exercise, and medications on endogenous DHEA and DHEAS levels.

 

Contraindications

 

DHEA supplementation is contraindicated in patients with a history of sex hormone-responsive cancers, such as breast, ovarian, endometrial, and prostate cancer. Women with a family history of postmenopausal, estrogen- sensitive cancers and men with benign prostatic hypertrophy or a family history of prostate cancer should carefully weigh the risks and benefits of DHEA replacement therapy with their physician. If replacement therapy is deemed necessary, close monitoring of serum DHEAS and its androgenic and estrogenic metabolites should be performed frequently. DHEA supplementation should be avoided during pregnancy and lactation.

 

Conclusion

 

Clinical data suggest that DHEA may have a role in hormone replacement therapy in patients with low endogenous DHEA and DHEAS levels due to chronic diseases, adrenal exhaustion, corticosteroid therapy, and advancing age. However, as a potent steroid precursor, DHEA can significantly increase androgen levels in women and may enhance the progression of estrogen and testosterone-sensitive cancers. Supplementation with DHEA should never be undertaken without direct medical supervision. The long-term effects of DHEA supplementation are unknown.

 

References

 

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Derksen RH. Dehydroepiandrosterone (DHEA) and systemic lupus erythematosus. Semin Arthritis Rheum. 1998; 27:335-47.

DHEA monograph. Natural Medicines Comprehensive Database. www.naturaldatabase. com (accessed 2000 May 6).

Morales AJ, Nolan JJ, Nelson JC et al. Effects of replacement dose of dehydroepiandrosterone in men and women of advancing age. J Clin Endocrinol Metab. 1994; 78:1360-7.

Baulieu EE, Thomas G, Legrain S et al. Dehydroepiandrosterone (DHEA), DHEA sulfate, and aging: contribution of the DHEAge study to a sociobiomedical issue. Proc Natl Acad Sci U S A. 2000; 97:4279-84.

Rabkin JG, Ferrando SJ, Wagner GJ et al. DHEA treatment for HIV+ patients: effects on mood, androgenic and anabolic parameters. Psychoneuroendocrinology. 2000; 25(1):53-68.

Reiter WJ, Pycha A, Schatzl G et al. Serum dehydroepiandrosterone sulfate concentrations in men with erectile dysfunction. Urology. 2000; 55:755-8.

Majewska MD, Demirgoren S, Spivak CE et al. The neurosteroid dehydroepiandrosterone sulfate is an allosteric antagonist of the GABA A receptor. Brain Res. 1990; 526: 143-6.

Migeon CJ, Keller AR, Lawrence B et al. Dehydroepiandrosterone and androsterone levels in human plasma. Effect of age and sex, day-to-day and diurnal variations. J Clin Endocrinol Metab. 1957; 17:1051-62.

Orentreich N, Brind JL, Vogelman JH et al. Long-term longitudinal measurements of plasma dehydroepiandrosterone sulfate in normal men. J Clin Endocrinol Metab. 1992; 75:1002-4.

Labrie F, Belanger A, Cusan L et al. Marked decline in serum concentrations of adrenal C19 sex steroid precursors and conjugated androgen metabolites during aging. J Clin Endocrinol Metab. 1997; 82:2396-402.

Bird CH, Masters V, Clark AF. Dehydroepiandrosterone sulfate: kinetics of metabolism in normal young men and women. Clin Invest Med. 1984; 7:119-22.

Poortman J, Andriesse R, Agema A et al. Adrenal androgen secretion and metabolism in post-menopausal women. In: Genazzani AR, Thijssen JH, Siiteri PK, eds. Adrenal androgens. New York: Raven; 1980:219-40.

Robel P, Baulieu EE. Dehydroepiandrosterone (DHEA) is a neuroactive neurosteroid. Ann N Y Acad Sci. 1995; 774:82-110.

Lacroix C, Fiet J, Benais J-P et al. Simultaneous radioimmunoassay of progesterone, androst-4-enedione, pregnenolone, dehydroepiandrosterone and 17-hydroxy-progesterone in specific regions of the human brain. J Steroid Biochem. 1987; 28: 317-25.

Morales AJ, Haubrich RH, Hwang JY et al. The effect of six months treatment with a 100 mg daily dose of dehydroepiandrosterone (DHEA) on circulating sex steroids, body composition and muscle strength in age-advanced men and women. Clin Endocrinol. 1998; 49:421-32.

Arlt W, Haas J, Callies F et al. Biotransformation of oral dehydroepiandrosterone in elderly men: significant increase in circulating estrogens. J Clin Endocrinol Metab. 1999; 84:2170-6.

Baulieu EE, Robel P. Dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS) as neuroactive neurosteroids. Proc Natl Acad Sci U S A. 1998; 95:4089-91.

Roberts E, Bologa L, Flood JF et al. Effects of dehydroepiandrosterone and its sulfate on brain tissue in culture and on memory in mice. Brain Res. 1987; 406:357-62.

Compagnone NA, Mellon SH. Dehydroepiandrosterone: a potential signalling molecule for neocortical organization during development. Proc Natl Acad Sci U S A. 1998; 95:4678-83.

Jakubowicz D, Beer N, Rengifo R. Effect of dehydroepiandrosterone on cyclic guanosine monophosphate in men of advancing age. Ann N Y Acad Sci. 1995; 774(Dec):312-5.

Jesse RL, Loesser K, Eich DM et al. Dehydroepiandrosterone inhibits human platelet aggregation in vitro and in vivo. Ann N Y Acad Sci. 1995; 774(Dec):281-90.

Beer N, Jakubowicz D, Matt DW et al. Dehydroepiandrosterone reduces plasma plasminogen activator inhibitor type 1 and tissue plasminogen activator antigen in men. Am J Med Sci. 1996; 311(5):205-10.

Alexandersen P, Haarbo J, Christiansen C. The relationship of natural androgens to coronary heart disease in males: a review. Atherosclerosis. 1996; 125(1):1-13.

Kiechl S, Willeit J, Bonora E et al. No association between dehydroepiandrosterone sulfate and development of atherosclerosis in a prospective population study (Bruneck study). Arterioscler Thromb Vasc Biol. 2000; 20:1094-100.

Casson PR, Andersen RN, Herrod HG et al. Oral dehydroepiandrosterone in physiological doses modulates immune function in postmenopausal women. Am J Obstet Gynecol. 1993; 169:1536-9.

Khorram O, Vu i, Yen SS. Activation of immune function by dehydroepiandrosterone (DHEA) in age-advanced men. J Gerontol A Biol Sci Med. 1997; 52(1):M1-7.

Straub RH, Konecna L, Hrach S et al. Serum dehydroepiandrosterone (DHEA) and DHEA sulfate are negatively correlated with serum interleukin-6 (IL-6), and DHEA inhibits IL-6 secretion from mononuclear cells in man in vitro: possible link between endocrinosenescence and immunosenescence. J Clin Endocrinol Metab. 1998; 83: 2012-7.

Longcope C. Dehydroepiandrosterone metabolism. J Endocrinol. 1996; 150(suppl): S125-7.

Bird CE, Murphy J, Boroomand K et al. Dehydroepiandrosterone: kinetics of metabolism in normal men and women. J Clin Endocrinol Metab. 1976; 47:818-22.

Zumoff BV, Bradlow HL. Sex difference in the metabolism of dehydroepiandrosterone sulfate. J Clin Endocrinol Metab. 1980; 51: 334-6.

Tummala S, Svec F. Correlation between the administered dose of DHEA and serum levels of DHEA and DHEA-S in human volunteers: analysis of published data. Clin Biochem. 1999; 32:355-61.

Van Vollenhoven RF, Engleman EG, McGuire JL. Dehydroepiandrosterone in systemic lupus erythematosus. Arthritis Rheum. 1995; 38:1826-31.

Van Vollenhoven RF. Dehydroepiandrosterone in systemic lupus erythematosus. Rheum Dis Clin North Am. 2000; 26:349-62.

Huppert FA, Van Niekerk JK, Herbert J. Dehydroepiandrosterone (DHEA) supplementation for cognition and well-being. Cochrane Database Syst Rev. 2000; 2:CD000304.

Berr C, Lafont S, Debuire B et al. Relationships of dehydroepiandrosterone sulfate in the elderly with functional, psychological, and mental status, and short-term mortality: a French community-based study. Proc Natl Acad Sci U S A. 1996; 93:13410-5.

Tordjman S, Anderson GM, McBride PA et al. Plasma androgens in autism. J Autism Dev Disord. 1995; 25:295-304.

Goodyer IM, Herbert J, Altham PME et al. Adrenal secretion during major depression in 8- to 16-year olds: I. Altered diurnal rhythms in salivary cortisol and dehydroepiandrosterone (DHEA) at presentation. Psychol Med. 1996; 25:245-56.

Herbert J, Goodyer IM, Altham PME et al. Adrenal secretion during major depression in 8- to 16-year olds: II. Influence of comorbidity at presentation. Pychol Med. 1996; 25:257-63.

Wolkowitz OM, Reus VI, Keebler A et al. Double-blind treatment of major depression with dehydroepiandrosterone. Am J Psychiatry. 1999; 156:646-9.

Christeff N, Lortholary O, Casassus P et al. Relationship between sex steroid hormone levels and CD4 lymphocytes in HIV infected men. Exp Clin Endocrinol Diabetes. 1996; 104(2):130-6.

Buster JE, Casson PR, Straughn AB et al. Postmenopausal steroid replacement with micronized dehydroepiandrosterone: preliminary oral bioavailability and dose proportionality studies. Am J Obstet Gynecol. 1992; 166:1168-70.

Dorgan JF, Stanczyk FZ, Longcope C et al. Relationship of serum dehydroepiandrosterone (DHEA), DHEA sulfate, and 5- androstene-3 beta, 17 betadiol to risk of breast cancer in postmenopausal women. Cancer Epidemiol Biomarkers Prev. 1997; 6 (3):177-81.

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http://www.medscape.com/viewarticle/465827_print

 

Low-Dose DHEA Increases Androgen, Estrogen Levels in Menopause

 

Mindy Hung

Medscape Medical News 2003. © 2003 Medscape

 

Dec. 12, 2003 — Low-dose dehydroepiandrosterone (DHEA) administration increases adrenal hormone plasma levels in early and late menopause, according to results of a prospective case study published in the December issue of Fertility and Sterility.

 

"Although DHEA supplementation is not yet considered a medical treatment, this steroid has been demonstrated to induce specific metabolic effects and to increase both androgen and estrogen plasma levels in postmenopausal women," write Alessandro D. Genazzani, MD, PhD, and colleagues from the University of Modena in Italy.

 

The Italian team selected 20 healthy, postmenopausal patients, age 50 to 65 years, who were not using hormone replacements, for the 12-month prospective study. All patients received an ultrasound examination and a mammogram before the start of the study to exclude organic disease.

 

Dr. Genazzani and colleagues divided patients by age into two groups: early (aged 50-55 years, n = 10, group A) who were two to three years postmenopausal; and late (aged 60-65 years, n = 10, group B) who were five or more years postmenopausal. Five of the women were mild smokers.

 

All patients took 25 mg/day DHEA supplementation for 12 months. Every three months throughout the trial period, the investigators evaluated patients and drew blood samples to determine plasma levels of LH, FSH, E2, DHEA, DHEAS, androstenedione (A), testosterone, dihydrotestosterone, progesterone, 17 alpha-hydroxyprogesterone (17-OHP), allopregnanolone, estrone (E1), sex-hormone binding globulin (SHBG), cortisol (F), beta-endorphin, growth hormone (GH), and insuline-like grown factor-1 (IGF-1).

 

Investigators also conducted a transvaginal ultrasound examination in each patient before and after 6 and 12 months of treatment to evaluate endometrial thickness. In addition, the researchers administered a Kupperman questionnaire to evaluate subjective vasomotor and psychological symptoms before and after 3, 6, and 12 months of therapy.

 

Younger postmenopausal subjects (group A) demonstrated higher levels of DHEA, DHEAS, testosterone, and beta-endorphin levels than older subjects (P < .05). Significant changes in endocrine levels were observed with therapy. DHEA treatment eliminated endocrine differences observed between the two groups at baseline.

 

Testosterone and dihydrotestosterone plasma levels, and plasma E1 and E2 levels increased significantly and progressively in both groups. Investigators found no changes in SHBG concentrations in either group despite significant changes in A and E plasma concentrations. Allopregnanolone and beta-endorphin concentrations significantly increased in both groups.

 

Cortisol F plasma levels progressively decreased throughout the study. Both groups also experienced significantly reduced LH and FSH plasma levels. GH and IGF-1 levels significantly increased in both groups. Supplementation did not induce changes in endometrial thickness.

 

At baseline, group A had higher values for subjective vasomotor disturbances and psychological disturbances than group B, whereas the latter had a higher score for psychological variables. Scores significantly improved in both groups during therapy.

 

"The present study demonstrates the efficacy of low-dose DHEA administration of endocrine and psychoneuroendocrine parameters in early and late menopause and confirms that a low-dose DHEA supplementation increases adrenal androgens plasma levels (mainly DHEA and DHEAS), which are significantly impaired during menopause," Dr. Genazzani and colleagues write.

 

"These data support and confirm that DHEA must be considered a valid compound and drug for [hormone therapy] in postmenopausal women and not just a 'dietary supplement,' " they add.

 

Fertil Steril. 2003;80:1495-1501

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http://www.webmd.com/content/article/100/105716.htm

 

DHEA May Help Midlife Depression

 

Conventional Antidepressants Still the First Line of Defense, Says Study

By Miranda Hitti

Reviewed By Brunilda Nazario, MD

 

WebMD Medical News

on Monday, February 07, 2005

 

Feb. 7, 2005 -- The hormonal supplement DHEA could help relieve mild to moderate depression that starts in middle age, new research shows.

 

Still, DHEA probably isn't the first option patients should consider, say the researchers. In their small study, treatment with DHEA resulted in a 50% reduction in depression symptoms in half the participants.

 

"With a 50% response rate, one would obviously select more reliable first-line treatments for this condition," write the researchers, who included Peter J. Schmidt, MD, of the National Institute of Mental Health (NIMH).

 

"However," the researchers write, "in the 50% of depressed outpatients who do not respond to first-line antidepressant treatments, or in those unwilling to take traditional antidepressants, DHEA may have a useful role in the treatment of mild to moderately severe midlife-onset major and minor depression."

 

Their findings appear in the February edition of the Archives of General Psychiatry.

 

Depression is Widespread

 

Every year, about 9% of the U.S. adult population -- nearly 19 million people -- have depression, says the NIMH. Women are affected twice as often as men, but depression can strike either sex at any age.

 

Depression can be devastating, grinding life to a crawl. It can make ordinary tasks seem overwhelming and robs patients of pleasures they once enjoyed. Depression also casts a long shadow over physical health, as mind and body are intertwined.

 

Depression is also highly treatable. Counseling, medication, and lifestyle changes can help tremendously. But for many people, the hardest part is reaching out for help. If patients only ask, doctors and therapists can often help find solutions to revive wellbeing.

 

A growing number of people are exploring alternatives to conventional antidepressants, say the researchers. Since DHEA has been reported to help soothe depression, Schmidt's team tested it against midlife depression.

 

About DHEA

 

DHEA is a naturally occurring steroid hormone that is a precursor to the male sex hormone testosterone and the female sex hormone estrogen.

 

Made by the adrenal glands, DHEA production dwindles starting in early adulthood. By age 70, DHEA production is about 20% of that in the late teens or early 20s.

 

DHEA supplements are widely available over the counter and on the Internet. Its popularity has been fueled by claims of antiaging effects, which has also attracted the interest of researchers.

 

But since the FDA doesn't regulate supplements, it's hard to know exactly what's being sold. That alarms some health experts, especially since people often take supplements without telling their doctors.

 

DHEA-Depression Study

 

The study was small and brief. It included 23 men and 23 women age 40 to 65 with mild to moderate depression starting in midlife. None was severely depressed or taking other antidepressants. Besides their depression, they were in good health.

 

Subjects were assigned to take either DHEA or a placebo for six weeks. After a 1-2 week break, the groups switched to the other pill for six more weeks.

 

Two DHEA doses were used. For three weeks, patients took a lower dose -- 90 milligrams per day. For the other three weeks, they took 450 milligrams of DHEA daily.

 

Less Depression with DHEA

 

In 23 participants, DHEA cut depression symptoms by 50% or more. A similar reduction was seen in 13 subjects after taking the placebo. Men and women responded similarly.

 

Treatment with the supplement was associated with an increase in testosterone blood levels in both men and women.

 

Taking DHEA for 6 weeks also significantly improved sexual function scores, compared to the scores after taking the placebo or before the study started.

 

DHEA was well tolerated. Acne and oily skin were the most common adverse effects.

 

Because of the study's design, its findings don't apply to severely depressed patients, say the researchers. They also warn that DHEA's long-term effects aren't known and that more studies are needed.

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http://www.ncbi.nlm.nih.gov/pubmed/9024954?dopt=Abstract

 

Biol Psychiatry. 1997 Feb 1;41(3):311-8.

 

Dehydroepiandrosterone (DHEA) treatment of depression.

 

Wolkowitz OM, Reus VI, Roberts E, Manfredi F, Chan T, Raum WJ, Ormiston S, Johnson R, Canick J, Brizendine L, Weingartner H.

 

Source

Department of Psychiatry, University of California, San Francisco, School of Medicine 94143-0984, USA.

 

Dehydroepiandrosterone (DHEA) and its sulfate, DHEA-S, are plentiful adrenal steroid hormones that decrease with aging and may have significant neuropsychiatric effects. In this study, six middle-aged and elderly patients with major depression and low basal plasma DHEA f1p4or DHEA-S levels were openly administered DHEA (30-90 mg/d x 4 weeks) in doses sufficient to achieve circulating plasma levels observed in younger healthy individuals. Depression ratings, as well as aspects of memory performance significantly improved. One treatment-resistant patient received extended treatment with DHEA for 6 months: her depression ratings improved 48-72% and her semantic memory performance improved 63%. These measures returned to baseline after treatment ended. In both studies, improvements in depression ratings and memory performance were directly related to increases in plasma levels of DHEA and DHEA-S and to increases in their ratios with plasma cortisol levels. These preliminary data suggest DHEA may have antidepressant and promemory effects and should encourage double-blind trials in depressed patients.

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http://www.medscape.com/viewarticle/522145

 

Medscape Medical News

 

DHEA May Be Effective for Depression Associated With HIV

 

News Author: Laurie Barclay, MD

 

Release Date: January 24, 2006

 

Jan. 24, 2006 — Dehydroepiandrosterone (DHEA) is an effective therapy for treatment of nonmajor depression in patients with HIV/AIDS, according to the results of a randomized trial reported in the January issue of the American Journal of Psychiatry.

 

"Subsyndromal major depressive disorder is common among HIV-positive adults," write Judith G. Rabkin, PhD, MPH, from the New York State Psychiatric Institute, Columbia University College of Physicians and Surgeons in New York, and colleagues. "DHEA is of particular interest for HIV-positive patients, because declining levels of DHEA have been associated with progression to AIDS in both cross-sectional comparisons of HIV-positive men and women at different stages of HIV illness and in longitudinal studies, including a previous study by our group."

 

In this 8-week trial, 145 patients with subsyndromal depression or dysthymia were randomized to receive either DHEA, using flexible dosing of 100 to 400 mg/day, or placebo. Study completion rates were 90% (69/77) of the DHEA-treated patients and 94% (64/6 of the placebo-treated patients. The primary efficacy endpoint, based on intent-to-treat analysis and completer analysis, was a Clinical Global Impression improvement rating of 1 or 2 (much or very much improved) plus a final Hamilton Depression Rating Scale (HAM-D) score of 8 or less. Safety outcomes included adverse effect reports and measures of CD4 cell count and HIV RNA viral load at baseline and at week 8.

 

In the intent-to-treat analysis, clinicians' ratings demonstrated that DHEA was superior, with response rates of 56% (43/77) for the DHEA group vs 31% (21/6 for the placebo group. In the completer analysis, response rates were 62% (43/69) for DHEA and 33% (21/ 64) for placebo. Based on intent-to-treat data, the number needed-to-treat was 4 vs 3.4 on the basis of completer data. There were few adverse events and no significant changes in CD4 cell count or HIV RNA viral load in either treatment group.

 

"Nonmajor but persistent depression is common in patients with HIV/AIDS, and DHEA appears to be a useful treatment that is superior to placebo in reducing depressive symptoms," the authors write. "The low attrition rate in this group of physically ill patients, together with requests for extended open-label treatment, reflect high acceptance of this readily available intervention."

 

Study limitations include lack of generalizability to patients with major depression or those with substance use disorders, small number of women, absence of long-term follow-up regarding maintenance of response or possible long-term endocrine or other effects of DHEA, and restriction of the study to HIV-positive individuals.

 

"Given the high acceptance rate and low side effect profile for DHEA in this group of patients with HIV/AIDS, nearly all of whom were taking multiple concurrent medications, it may be appropriate to evaluate the efficacy of DHEA in other groups of physically ill patients in which mild depression is common," the authors conclude. "We do not recommend widespread use of DHEA in the absence of confirmatory efficacy research and more data about longer-term use. For patients who are unwilling to take antidepressants, who express a strong preference for an 'alternative' treatment, and who have nonmajor depression, DHEA may be a reasonable choice."

 

The National Institutes of Mental Health supported this study.

 

Am J Psychiatry. 2006;163:59-66

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Hormone may combat mid-life depression - study

 

Last Updated: 2005-02-07 16:00:32 -0400 (Reuters Health)

 

CHICAGO (Reuters) - ....The supplement DHEA -- dehydroepiandrosterone -- "may have a useful role in the treatment of mild to moderately severe midlife-onset major and minor depression" in some patients, said the report from the National Institute of Mental Health.

 

The findings were based on a small study involving 46 men and women aged 45 to 65 who had major or minor depression of moderate severity.

 

Some were given the drug and others an inert placebo, and the process was repeated switching the drug and no-drug groups. At the end the participants were measured by standard tests for depression.

 

In all, 23 showed a reduction of at least 50 percent in their depression after they received the drug. In addition, 13 showed improvement after the placebo.

 

The report was published in the Archives of General Psychiatry.

 

The authors said since only half of those studied found improvement with the drug and it is not clear why or for whom it best works, a more conventional anti-depression drug would likely the first choice for treatment.

 

But for those patients who do not respond to such drugs or are unwilling to take them, DHEA may be useful, it added.

 

DHEA, a hormone produced by the adrenal glands, is widely touted on the Internet and elsewhere as a "fountain of youth" drug that can slow the aging process.

 

SOURCE: Archives of General Psychiatry, February 2005.

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I did try DHEA myself. It helped my sleep and, apparently, my post-SSRI sexual disorder (PSSD) anorgasmia.

 

My notes from 2006:

 

3/18/06 Tests show I have low DHEA so I just started taking it.

 

I started out a few days ago with 2.5mg/day, supposed to be an insignificant amount. I thought it was making me sleepy, but otherwise no effects.

 

I took 5mg (a physiological dose) this morning and I feel....sleepy. I'm not adverse to something making me feel sleepy, I need to sleep better. I'm going to take it at night from now on. But does this make sense that DHEA makes me sleepy?

 

-----

3/20/06

Took 5mg DHEA at bedtime last night and got a good night's sleep, which has been very rare in the last 16 months of discontinuation syndrome.

 

Feel very calm, but not groggy, this morning.

 

-----

3/20/06

I wouldn't suggest everyone take DHEA; I've had a couple of tests and my DHEA level has been very low for more than a year, so supplementation makes sense for me.

 

The endocrinologist who prescribed DHEA for me has an "integrative" practice. When I mentioned treatment with tiny amounts of amino acids or hormones to my conventional endocrinologist, he was against it. He considers 5mg DHEA to be a "homeopathic" dose.

 

Conventional or allopathic endocrinologists look for severe disease conditions before they offer treatment. They're not inclined to do subtle tune-ups; they bring in the heavy machinery. Consequently, they think in terms of very large doses, which probably are too much of a shock to the system.

 

All the same, I think I'll just take 2.5mg DHEA tonight to see if it makes me drowsy enough.

 

-----

3/23/06

Yep, 2.5mg DHEA was plenty, made me groggy -- I cut back to 1.25mg DHEA at night and it seems to get me to sleep. Mood is stable.

 

DHEA increases the effect of GABA. Sedatives and sleep drugs like Ambien tend to be GABA-ergics.

 

DHEA is supposed to cut appetite, but I'm eating everything I can find. This is a good thing, I guess, because until recently I had no appetite and lost a lot of weight pretty quickly.

 

-----

3/23/06 Note to insomniacs: I started taking a minute amount of DHEA, which my tests said was low. I take 1.25-2.5mg at night, and it helps me sleep!)

 

Discontinuation syndrome also made me hypersensitive to vitamins, supplements, medications, even food. I'm just really, really careful about what I take now -- that's why I started with 2.5mg DHEA instead of the 5mg my doctor recommended, and I cut back to 1.25mg because that seems like enough.

 

PS I'm of the female persuasion.

 

-----

3/25/06

I definitely think DHEA has helped me sleep. I'm sleeping so soundly now that I don't wake up to pee until morning. DHEA is also a cortisol fighter.

 

I'm cutting 5mg tabs into quarters to get 1.25mg doses. I think I saw 5mg tabs in Pharmaca. I would phone the high-end health food stores to find it.

 

More info on DHEA: http://www.womentowomen.com/adrenalhealth/dhea-naturalandsupplementation.aspx

 

-----

7/4/06

Still getting good results from DHEA, taking 7.5mg at night.

 

-----

7/22/06

Went up to 10mg DHEA, 5mg in the morning and 5mg at night, and all seemed to be well for a week or so.

 

Then I started to get acne on my chin and had a bout of severe insomnia for a couple of weeks. I don't know if the increased DHEA was responsible for the insomnia, but I cut back to 5mg and am sleeping better. Acne cleared up.

 

A doc told me DHEA is converted in women to testoterone. (From what I've read, some of the testosterone can be converted into estrogen.) I do believe the higher dose enhanced my sex drive, such as it is.

 

-----

8/13/06

Took DHEA 5mg by mistake this morning -- I usually take 5mg at night and 2.5mg in the morning for a total of 7.5mg/day. The extra dosage made me sleepy, dammit. Guess I'm not gonna be that productive today.

 

-----

October 2006

Right, when I started taking a bit of DHEA in the evening (eventually 5mg), it helped me sleep, which was a real relief from discontinuation insomnia!

 

I also take 2.5mg DHEA in the morning.

 

DHEA converts to testosterone and possibly estrogen, so it is not recommended for people young enough to have their own peak amounts of testosterone or estrogen, or for women who are pregnant or intending to be. DHEA declines quite a bit after 40 years of age, so it's safer to take it when you're an older person.

 

I personally believe it's a good alternative to conventional hormone therapy for symptoms of menopause.

 

-----

December 2006

 

Please note that I take only 7.5mg DHEA and, yes, that small amount does make my skin oily, gives me a little acne, and has increased my libido.

 

I would start with a very small dose and see how you do with that.

 

-----

1/22/08 [i started to see my current doctor.] He advised me to temporarily reduce Seriphos (phosphatidylserine), folate (metafolin), and DHEA as these can be stimulating.

 

-----

5/3/08 Just for the record, I want to report here sexual sensation gradually came back after a couple of years and orgasm improved but, 42 months post-Paxil, has not yet returned to normal. As I am menopausal, I found DHEA helped some but since I stopped it I would say orgasm is only about 50 percent of normal.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

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Alto -

 

I've only skimmed these posts, but after skimming AND reading your diary entries in the last post, I continue to be blown away by how courageous and strong you have been. And not to mention assiduous to your cause of getting the word out about possible treatments and, of course, the dark side of SSRIs.

 

Amazing. I hope some day all your knowledge can be compiled into an anthology-type textbook co-authored with other psychiatrists (Dr Prey!) and neurologists about how to treat SSRI discontinuation and restore the mind/body back to health.

Been on SSRIs since 1998:

1998-2005: Paxil in varying doses

2005-present: Lexapro.

2006-early '08: Effexor AND Lexapro! Good thing I got off the Effexor rather quickly (within a year).

 

**PSYCHIATRY: TAKE YOUR CHEMICAL IMBALANCE AND CHOKE ON IT!

APA=FUBAR

FDA=SNAFU

NIMH=LMFAO

 

Currently tapering Lexapro ~10% every month:

 

STARTING: 15 mg

11/7/10: 13.5 mg

12/7/10: 12.2 mg

1/6/11: 10.9 mg

2/3/11: 9.8 mg

3/3/11: 8.8 mg

4/1/11: 7.8 mg

4/29/11: 7 mg

5/27/11: 6.4 mg

6/24/11: 5.7 mg

7/22/11: 5 mg

8/18/11: 4.5 mg

9/14/11: 4 mg

10/13/11: 3.6 mg

11/9/11: 3.2 mg

12/7/11: 2.6 mg

1/3/12: 2.1 mg

2/2/12: 1.8 mg

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Oh, thanks, cine, for your encouragement.

 

I'm sure there are those who would just rather I shut up! It was very sad for me to retrieve those posts from Google cache because they've been deleted from where they were originally posted.

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

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  • 7 months later...

I recently started thinking about DHEA again because I came across an article that said DHEA can increase your fertility: http://www.sciencedaily.com/releases/2010/07/100701145535.htm

 

Most of the studies are in relation to in vitro fertilization, like this one: http://www.rbej.com/content/7/1/108

 

If this can help me get pregnant AND help with depression and sleep, that would be incredible. But, I'm too scared to take it. I think I'm going to go to a fertility specialist I went to before and ask him to check my DHEA levels. He'll probably think that is weird, though, I think he's pretty conventional.

'94-'08 On/off ADs. Mostly Zoloft & Wellbutrin, but also Prozac, Celexa, Effexor, etc.
6/08 quit Z & W after tapering, awful anxiety 3 mos. later, reinstated.
11/10 CTed. Severe anxiety 3 mos. later & @ 8 mos. much worse (set off by metronidazole). Anxiety, depression, anhedonia, DP, DR, dizziness, severe insomnia, high serum AM cortisol, flu-like feelings, muscle discomfort.
9/11-9/12 Waves and windows of recovery.
10/12 Awful relapse, DP/DR. Hydrocortisone?
11/12 Improved fairly quickly even though relapse was one of worst waves ever.

1/13 Best I've ever felt.

3/13 A bit of a relapse... then faster and shorter waves and windows.

4/14 Have to watch out for triggers, but feel completely normal about 80% of the time.

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Please, everyone, be careful with DHEA.

 

In women, it increases androgen (male sex hormones) -- often you get whiskers. This is too much androgen. It's unbalancing your hormones.

 

The androgen can be activating, keeping you awake or making you agitated.

 

For women, 50mg DHEA is a very high dosage. (I got whiskers taking 2.5mg DHEA.)

 

Unless you are under the care of a knowledgeable doctor, women shouldn't take any more than 5mg, see http://www.raysahelian.com/dhea.html (Despite his selling supplements, Dr. Sahelian is a fairly reliable source for supplement info.)

 

DO NOT EXCEED more than 5 mg a day on a long term basis. Blood and saliva testing are not reliable ways to determine how much DHEA you should take because blood levels do not give a clear view on how this hormone is interacting within cells in the brain, skin, hair, liver, breast, prostate, and other tissues and organs. You may consider other non-hormonal options to improve your health.....If there are no other good options, and if you really do need to take a DHEA supplement, use the smallest amount that works in order to prevent unpleasant reactions. Take frequent breaks which I call 'hormone holidays.'

 

Also see this discussion in tezza's topic http://survivingantidepressants.org/index.php?/topic/1644-tezza-risperdal-withdrawal/page__view__findpost__p__19058

This is not medical advice. Discuss any decisions about your medical care with a knowledgeable medical practitioner.

"It has become appallingly obvious that our technology has surpassed our humanity." -- Albert Einstein

All postings © copyrighted.

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Alto I take bio-identical hormones. Estradiol (tablet) and Progesterone/

Testosterone cream (compounded).

 

Initially I had DHEA in the Prog/Test Cream, but I had it removed because it can cause anxiety. I spoke to a few other women I worked with at the time and they said DHEA is known for causing anxiety.

 

I am so prone to anxiety I suppose anything can add to it.

 

Hugs

Intro: http://survivingantidepressants.org/index.php?/topic/1902-nikki-hi-my-rundown-with-ads/

 

Paxil 1997-2004

Crossed over to Lexapro Paxil not available

at Pharmacies GSK halted deliveries

Lexapro 40mgs

Lexapro taper (2years)

Imipramine

Imipramine and Celexa

Now Nefazadone/Imipramine 50mgs. each

45mgs. Serzone  50mgs. Imipramine

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  • 8 months later...
  • 3 years later...

Do you happen to know why DHEA is not recommended for older men > 60 yo?

If on a Benzo for a relatively short period of time, such as less than 6-12 months, one may want to consider tapering off their Benzo first (please see Will Hall's book on Harm Reduction)

 

Prior to commencing with an AD taper please consider what problems the AD is causing, as tapering is an extremely serious endeavor.   

If one has been on an AD for more than 10 yrs. please consider the potential long term negative consequences of AD withdrawal prior to tapering. (please see Drs. Healy, Glenmullen and Shipko) 

Prior to re-starting an AD taper, please do not resume tapering until all w/d sx's from any prior taper, especially CT, have resolved. 

 

2004 - Dec. 2015,  Cymbalta 20mg/d  for neck pain - Never had problems with Cymbalta.   Dec 2015, CT 20mg/d Cymbalta.  5 weeks later reinstated 20mg/d Cymbalta - without increase in CT sx's.   

Feb 2016 STARTED VALIUM 25mg/d for CT Cymbalta wd sxs.    Jan-April 2016 Held Cymbalta 20mg/d - doing pretty well (AM 3/10 anxiety and 3/10 tinnitus)

April 2016, CT Cymbalta sx's had not yet resolved and I prematurely tapered 10% q 4 wks x 3 mos.  After 3rd cut developed 10/10 wd sx's of Anxiety, Anhedonia, Anorexia, Panic attacks, dark, incresaed Valium to 28mg/d. 

November 2016, after 3 cuts, UP-DOSED all (41 beads) back up to 20mg (193 beads total) Cymbalta - from , dark to light.

VALIUM TAPER: Jan 2017 28mg to March 2019 Zero   Cymbalta has partially stabilized and helped with the Valium taper.  The only sx I have now is 3/10 Tinnitus, which I only notice when it is quiet.

http://survivingantidepressants.org/index.php?/topic/11900-woof-cymbalta-re-stabilization-after-cold-turkey-withdrawal/  Benzo Posts http://survivingantidepressants.org/index.php?/topic/11951-woof-valium-scheduling-and-dosage-with-cymbalta-wd-symptoms/

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